Nelesen R A, Dimsdale J E, Mills P J, Clausen J L, Ziegler M G, Ancoli-Israel S
Department of Psychiatry, University of California, San Diego, USA.
Sleep. 1996 Feb;19(2):139-44. doi: 10.1093/sleep/19.2.139.
Adrenergic regulation in sleep apnea is a complex process because adrenergic physiology is difficult to summarize with one measure. Furthermore, the role of the adrenergic system in sleep apnea is often confounded with hypertension, making interpretation difficult in hypertensive apneics. Sixty-six people with and without apnea and/or hypertension (all were off antihypertensive medication) participated in this study. Cardiac beta-adrenergic drive, as assessed by systolic time intervals, was examined at rest and in response to a mild laboratory stressor. These measures of cardiac contractility included the pre-ejection period, electrical systole (QT) interval and the cardiac acceleration index. At rest, apneics showed elevated myocardial contractility on all measures (p = 0.001). In response to the laboratory stressor, non-apneics showed an increase in cardiac beta-adrenergic drive (p = 0.001), whereas the contractility in apneics did not change or decreased relative to baseline. These findings suggest disrupted cardiac adrenergic regulation in people with sleep apnea. Apnea appears to increase resting sympathetic activity and down regulate beta2-adrenergic receptors. The downregulation of cardiac beta-adrenergic receptor activity may explain the inability of people with sleep apnea to respond with appropriate cardiac contractility to a mild perturbation.
睡眠呼吸暂停中的肾上腺素能调节是一个复杂的过程，因为肾上腺素能生理学很难用一种测量方法来概括。此外，肾上腺素能系统在睡眠呼吸暂停中的作用常常与高血压混淆，这使得在高血压性呼吸暂停患者中进行解释变得困难。66名有或无呼吸暂停和/或高血压的人（均未服用抗高血压药物）参与了这项研究。通过收缩期时间间期评估的心脏β-肾上腺素能驱动在静息状态下以及对轻度实验室应激源的反应中进行了检查。这些心脏收缩力的测量指标包括射血前期、电收缩期（QT）间期和心脏加速指数。在静息状态下，呼吸暂停患者在所有测量指标上均表现出心肌收缩力升高（p = 0.001）。对实验室应激源的反应中，非呼吸暂停患者表现出心脏β-肾上腺素能驱动增加（p = 0.001），而呼吸暂停患者的收缩力相对于基线没有变化或下降。这些发现表明睡眠呼吸暂停患者存在心脏肾上腺素能调节紊乱。呼吸暂停似乎会增加静息交感神经活动并下调β2-肾上腺素能受体。心脏β-肾上腺素能受体活性的下调可能解释了睡眠呼吸暂停患者无法对轻度扰动做出适当的心脏收缩反应。
